Cancer is DEAD: Cancer cures from A to Z

How nice of you to tell potentially terminal people to stick it out with the Doc's narrow approaches after they've been told they have a short time
left to live. Rock on, eh.

Gee...I must have missed the part where I said that.

My point has always been that early treatment is essential, and that time spent self-medicating with complementary therapy might just lose you that
window of opportunity. Unfortunately, the pay-off for that choice is generally either death or much more invasive/debilitating treatment. I don't
hear you taking reponsibility for that.

You have plenty of folks on ATS that survived cancer using traditional medicine. How many have...themselves...beaten cancer using complementary
means?

Originally posted by JohnnyCanuck
Depriving people of that opportunity by distracting them with UNPROVEN therapies is morally reprehensible.

There you're insinuating that by listing a massive thing like I've done here I'm committing a moral crime...

...even though you can't quote me as saying people shouldn't listen to their doctors at all.

nd that time spent self-medicating with complementary therapy might just lose you that window of opportunity.

Now you're using the word "complimentary", while you've been insinuating that I'm telling people to go all out alternative / holistic. Perhaps
you need a reminder of the meaning of the word 'complimentary'?

You have plenty of folks on ATS that survived cancer using traditional medicine. How many have...themselves...beaten cancer using complementary
means?

The sound of crickets chirping is indeed your answer.

Gee... start a thread. Watch me: how many people have survived cancer? This deep in the thread, I'd be surprised if anyone notices me say that. Even
if anyone does, then again you'll be hard pressed to find anyone that knew all of these in advance, knew how to use them in advance, applied
it early stages and was willing to take the gamble.

The point isn't that people should gamble to appease your challenge... the point is your attack on my 'unscience' is itself unscientific.

Your words on the last page really seem like flannel chest pounding against complimentary treatments. Let me review your work in this
thread...

Originally posted by JohnnyCanuck
It is far too easy to shout about medical conspiracies and the suppression of wonder drugs...when you're healthy.

Oh? They told my mom her tumor is inoperable, and she has about a year to live. What did they do when she was in the hospital getting charged $10,000
(USD) per day? Fed her boiled broccoli that she couldn't eat even though she likes broccoli. By the time she went home: they didn't even tell her to
eat things like berries.

Originally posted by JohnnyCanuck
You are certainly not the only one on board with that story. One really big fear is that folks with their cancer at a treatable point ignore their
oncologists and seek alternative means, instead...and when they don't work, it's too late to treat by any means.

In the couple of months between diagnosis of my prostate cancer and my radiation treatment I used complementary medicine to try and bring down my
PSA...to no avail. I had the brachytherapy and the cancer is gone...and because it was caught early and the treatment highly focused, there's none of
that pesky incontinence and erectile dysfunction. They don't tell you that part when they're telling you to ignore your medical team and eat these
apricot pits instead.

By the way, an herbal preparation called zyflamend is in clinical trials for cancer treatment right now. How does that factor into the
conspiracy?

Hmm. So you attempted alternative therapy, over the period of a couple months, and it wasn't too late afterwards?

Tell us, what did you try, and how much?

It obviously wasn't too late for you. Did the cancer stop/slow in proliferation? That would be an item of discussion. If the alternative
treatments actually slowed the growth, that is grounds for using them as complimentary treatment.

And what's that, an herbal concoction is in clinical trials? Not according to: clinicaltrials.gov...
20 entries appear for the first one on my list that came to mind: curcumin.

Cyclooxygenase (COX) inhibitors have suppressive effects on several types of cancer cells including prostate cancer. In this study, we considered
the potential COX-inhibitory activity of a unique anti-inflammatory herbal preparation (Zyflamend; New Chapter, Inc., Brattleboro, VT) and analyzed
its effects on the human prostate cancer cell line LNCaP. COX inhibitory activity of Zyflamend was determined by a spectrophotometric-based assay
using purified ovine COX-1 and COX-2 enzymes. Effects of Zyflamend on LNCaP cell growth and apoptosis in vitro were assessed by cell counting, Western
blot detection of poly ADP-ribose polymerase (PARP) cleavage, and measurement of caspase-3 activity in treated and control cell extracts.

The multiherb anti-inflammatory product Zyflamend was investigated for its antiproliferative effects on PC3 human prostate cancer cells and
eicosanoid metabolism in this prostate cancer cell line. Zyflamend produced a concentration-dependent inhibition of cloned COX-1, COX-2, and 5-LOX
enzyme activities, with inhibition of 5-HETE production being greater than that of PGE(2) formation. Applied to intact PC3 cells, Zyflamend was found
to be most potent against 12-LOX, followed by 5-LOX and then COX activities. The concentration-dependent inhibition of PC3 cell proliferation was
associated with a selective G(2)/M arrest of the cell cycle and induction of apoptosis, as evidenced by flow cytometric staining of PC3 cells with
annexin V. Zyflamend also produced a concentration-dependent down-regulation of 5-LOX and 12-LOX expression.

Zyflamend, a polyherbal preparation, was designed based on constituents that exhibit antiproliferative, antiinflammatory, antioxidant,
antiangiogenic, and apoptotic activities through a mechanism that is not well defined. Because the nuclear factor (NF)-kappaB has been shown to
regulate proliferation, invasion, and metastasis of tumor cells, we postulated that Zyflamend modulates the activity of NF-kappa B. To test this
hypothesis, we examined the effect of this preparation on NF-kappaB and NF-kappaB-regulated gene products. We found that Zyflamend inhibited receptor
activator of NF-kappa B ligand-induced osteoclastogenesis, suppressed tumor necrosis factor (TNF)-induced invasion, and potentiated the cytotoxicity
induced by TNF and chemotherapeutic agents, all of which are known to require NF-kappa B activation. Zyflamend suppressed NF-kappa B activation
induced by both TNF and cigarette smoke condensate.

Good find!

That looks an awful lot like many of my entries (except the part where under each entry each citation shows results in different types of cancer
only).

Note that a great many of the entries in my list aren't merely in vitro successes.

Did you actually read my OP? I don;t think you did. You asked for a success story? Forget ATS, try NIH... I've been saving this for last: Possible disease remission in patient with invasive bladder cancer with D-fraction regimenwww.ncbi.nlm.nih.gov...

This case study describes an invasive bladder cancer patient at a high risk for disease recurrence who only followed a D-fraction regimen (with
vitamin C) refusing other medical interventions. The two-year follow-up yet indicated no clinical evidence of progression of residual disease or
recurrence with possible disease remission.

The bottom line is that the best bet we have in treating cancer is with the current medical practice. To postpone that treatment by using alternative
therapies can be a death sentence. By all means, eat well, use preventative measures, but when the doctor says "This radiation treatment will cure
you", in my estimation, only a fool will decline and keep sucking back the ol' essiac, et al.

That is the point that fails to come forward in discussions like this, and probably kills more cancer patients than alternative proponents would care
to know about.

Originally posted by IgnoranceIsntBlisss
So now you're not going to describe for us the alternative regimen you self-medicated with, and whether or not it slowed / stopped the
growth?

No, because I have done that a number of times on this site. I adopted a regimen recommended by a naturopath, all good stuff, and if it slowed my
prostate cancer in the time between a suspicion and the eventual procedure...well, it sure didn't show. I gave it 3 months then had the radioactive
implants. Waiting longer would have lost me that therapy and left me with more invasive options that generally end up involving incontinence and ED.

As far as I'm concerned...that's a pretty good example of the kind of bet upon the table, and you don't hear it enough in threads of this nature.
One final thought from me...unless one has actually faced a diagnosis of cancer, one has NO freakin' idea of what choice one would make. Over and
out.

Piperine
Natural Sources: Peppercorns.
Concentrated Sources: Marketed as "Bioperine". en.wikipedia.org...
It's what gives "Black Pepper" its taste. I found studies talking about combining it with curcumin treatments because it's known to help nutrient
uptake, and doing a scholar search I found multiple cancer studies using it alone.

Cytoprotective effect of piperine against benzoapyrene induced lung cancer with reference to lipid peroxidation and antioxidant system in
Swiss albino micewww.ncbi.nlm.nih.gov...

Piperine Enhances the Bioavailability of the Tea Polyphenol Epigallocatechin-3-gallate in Micejn.nutrition.org...

Epigallocatechin-3-gallate (EGCG), from green tea (Camellia sinensis), has demonstrated chemopreventive activity in animal models of
carcinogenesis. Previously, we reported the bioavailability of EGCG in rats (1.6%) and mice (26.5%). Here, we report that cotreatment with a second
dietary component, piperine (from black pepper), enhanced the bioavailability of EGCG in mice.

Effect of piperine on the inhibition of lung metastasis induced B16F-10 melanoma cells in mice www.springerlink.com...

The effect of piperine on the inhibition of lung metastasis induced by B16F-10 melanoma cells was studied in C57BL/6 mice. Simultaneous
administration of the compound with tumor induction produced a significant reduction (95.2%) in tumor nodule formation. Increased lung collagen
hydroxyproline (22.37 μg/mg protein) in the metastasized lungs of the control animals compared to normal animals (0.95 μg/mg protein) was
significantly reduced (2.59 μg/mg protein) in the piperine-treated animals. The high amount of uronic acid (355.83 μg/100 mg tissue) in the
metastasized control animals was significantly reduced (65 μg/100 mg tissue) in the animals treated with piperine. Lung hexosamine content was also
significantly reduced in the piperine-treated animals (0.98 mg/100 mg lyophilized tissue) compared to the untreated tumor-bearing animals (4.2 mg/100
mg lyophilized tissue). The elevated levels of serum sialic acid and serum gamma glutamyl transpeptidase activity in the untreated control animals was
significantly reduced in the animals treated with piperine. The piperine-treated animals even survived the experiment (90 days). Histopathology of the
lung tissue also correlated with the lifespan of the drug-treated animals. Our results demonstrate the antimetastatic activity of piperine, an
alkaloid present in plants such as Piper nigrum and Piper longum.

Piperine, a major ingredient of black and long peppers, protects against AFB1-induced cytotoxicity and micronuclei formation in H4IIEC3 rat
hepatoma cellswww.ncbi.nlm.nih.gov...

We studied the effect of piperine on the cytotoxicity and genotoxicity of aflatoxin B1 (AFB1) in rat hepatoma cells H4IIEC3/G-(H4IIE) using
cellular growth and formation of micronuclei as endpoints. Piperine was earlier shown to inhibit cytochrome P-450-dependent aryl hydrocarbon
hydroxylase and 7-methoxycoumarin demethylase activities in preparations of these cells with 1/2 maximum inhibition at 30-50 microM (Singh J. and Reen
R.K., Current Science, 66, 365-369, 1994). The results of the present study showed that AFB1 inhibited the growth of H4IIE cells with an ED50 of 15
nM. Piperine markedly reduced the toxicity of the mycotoxin. Thus at 100 microM piperine largely restored the rate of growth of the cells. Likewise,
piperine reduced the AFB1-induced formation of micronuclei in a concentration-dependent manner. Piperine itself was not toxic to the cells up to a
concentration of almost 100 microM. The results suggest, that piperine is capable of counteracting AFB1 toxicity by suppressing cytochromes P-450
mediated bioactivation of the mycotoxin.

In order to determine whether the dietary polyphenols, curcumin, and piperine are able to modulate the self-renewal of normal and malignant breast
stem cells, we examined the effects of these compounds on mammosphere formation, expression of the breast stem cell marker aldehyde dehydrogenase
(ALDH), and Wnt signaling. ...Curcumin and piperine separately, and in combination, inhibit breast stem cell self-renewal but do not cause toxicity to
differentiated cells. These compounds could be potential cancer preventive agents.

Parthenolide, an active ingredient of herbal remedies such as feverfew (tanacetum parthenium), mimicked the effects of IkappaBalpha by inhibiting
NF-kappaB DNA binding activity and Mn-SOD expression, and increasing paclitaxel-induced apoptosis of breast cancer cells. These results suggest that
active ingredients of herbs with anti-inflammatory properties may be useful in increasing the sensitivity of cancers with constitutively active
NF-kappaB to chemotherapeutic drugs.

Parthenolide is one of the main components responsible for the anti-inflammatory property of Feverfew. Recently, parthenolide has shown to induce
apoptosis in cancer cells. Here we further studied the mechanism of parthenolide-induced apoptosis by focusing on the role of intracellular thiols and
calcium in a human colorectal cancer cell, COLO 205. Parthenolide rapidly depleted intracellular thiols, including both free glutathione (GSH) and
protein thiols. Concomitantly, there were dose- and time-dependent increases in intracellular reactive oxygen species (ROS) and calcium levels.
Increased expression of GRP78 protein, a marker for endoplasmic reticulum stress was also detected. All these changes preceded parthenolide-induced
apoptotic cell death. More importantly, pretreatment with N-acetylcysteine, a precursor of GSH synthesis, protected the cells from
parthenolide-induced thiol depletion, ROS production, cytosolic calcium increase and completely blocked parthenolide-induced apoptosis. On the
contrary, pretreatment of buthionine sulfoximine, an inhibitor of GSH synthesis sensitized the cell to apoptosis. These data clearly demonstrate that
the intracellular thiols and calcium equilibrium play a critical role in parthenolide-induced apoptotic cell death.

Suppressed NF-kappaB and sustained JNK activation contribute to the sensitization effect of parthenolide to TNF-alpha-induced apoptosis in
human cancer cellswww.ncbi.nlm.nih.gov...

Our study revealed a new mechanism that PN inhibits TNF-alpha-mediated NF-kappaB activation via disrupting the recruitment of the IkappaB kinases
(IKK) complex to TNF receptor, which then blocked the subsequent signaling events including IKK kinase activation, IkappaBalpha degradation, p65
nuclear translocation, DNA binding and transactivation. Moreover, PN also markedly enhanced and sustained TNF-alpha-mediated JNK activation. A
specific JNK inhibitor (SP600125), as well as over-expression of dominant-negative forms of JNK1 and JNK2 abolished the sensitization effect of PN on
TNF-alpha-induced apoptosis. It is thus believed that suppressed NF-kappaB activation and sustained JNK activation contribute to the sensitization
effect of PN to TNF-alpha-mediated cell death in human cancer cells.

Parthenolide (PN) is a major sesquiterpene lactone of feverfew (Tanacetum parthanium) with known anti-inflammatory activity. However, the
anticancer effects of PN have not been well studied. In the present investigation, we examined the cancer chemopreventive property of PN using a
combination of in vivo and in vitro approaches. ...More importantly, we found that impaired AP-1, JNK and p38 signaling led to the sensitization of
JB6 cells to UVB-induced apoptosis. Data from our study for the first time confirm the anticancer property of PN in an animal model, and provide
evidence that the inhibitory effects on AP-1 and mitogen-activated protein kinases serve as one of the underlying mechanisms for the cancer
chemopreventive property of PN.

Fenretinide (N-4-hydroxyphenyl retinamide, 4HPR) is a synthetic anticancer retinoid that is a well-known apoptosis-inducing agent. Recently, we
observed that the apoptosis induced by fenretinide could be effectively enhanced in hepatoma cells by a concomitant treatment with parthenolide, which
is a known inhibitor of nuclear factor-kappaB (NF-kappaB). ...Compared with controls treated with an empty vector or with antisense cDNA, the ectopic
expression of ANKRD1 led to reduced colony formation and to enhanced apoptotic cell death in hepatoma cells. These results suggest that ANKRD1 and the
other genes, whose expressions were substantially modulated by the parthenolide-mediated inhibition of NF-kappaB activation, play roles in the
enhanced drug-induced apoptosis. In addition, this study suggests that those identified genes may be useful in anticancer strategies against
hepatoma.

Activation of the transcription factor nuclear factor-κB (NF-κB) has been implicated in pancreatic tumorigenesis. We evaluated the effect of a
novel NF-κB inhibitor, parthenolide, a sesquiterpene lactone isolated from the herb feverfew, in three human pancreatic tumor cell lines (BxPC-3,
PANC-1, and MIA PaCa-2). Parthenolide inhibited pancreatic cancer cell growth in a dose-dependent manner with substantial growth inhibition observed
between 5 and 10 μmol/L parthenolide in all three cell lines.

Parthenolide is a major sesquiterpene lactone derived from feverfew (Tanacetum parthenium) with known anti-inflammatory activity. Moreover, the
anticancer potential of this compound was suggested. In this study, we determined the effect of parthenolide on proliferation of three human cancer
cell lines: human lung carcinoma (A549), human medulloblastoma (TE671), human colon adenocarcinoma (HT-29) and human umbilical vein endothelial cells
(HUVEC) in vitro. Cell proliferation was assessed by means of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The IC(50)
value (the concentration of drug necessary to induce 50% inhibition) together with confidence limits was calculated. Parthenolide inhibited
proliferation of all three types of cancer cells (A549, TE671, HT-29) and HUVEC with the following IC(50) values (in muM): 4.3, 6.5, 7.0 and 2.8,
respectively. Thus, the antiproliferative potential of parthenolide was confirmed.

We have studied the in vitro actions of the sesquiterpene lactone parthenolide (PTL) on cells isolated from patients with chronic lymphocytic
leukemia (CLL). Dye reduction viability assays showed that the median LD50 for PTL was 6.2 M (n=78). Fifteen of these isolates were relatively
resistant to the conventional agent chlorambucil but retained sensitivity to PTL. Brief exposures to PTL (1–3 h) were sufficient to induce caspase
activation and commitment to cell death. Chronic lymphocytic leukemia cells were more sensitive towards PTL than were normal T lymphocytes or CD34+
haematopoietic progenitor cells. The mechanism of cell killing was via PTL-induced generation of reactive oxygen species, resulting in turn in a
proapoptotic Bax conformational change, release of mitochondrial cytochrome c and caspase activation. Parthenolide also decreased nuclear levels of
the antiapoptotic transcription factor nuclear factor-kappa B and diminished phosphorylation of its negative regulator IB. Killing of CLL cells by PTL
was apparently independent of p53 induction. This is the first report showing the relative selectivity of PTL towards CLL cells. The data here warrant
further investigation of this class of natural product as potential therapeutic agents for CLL.

parthenolide suppresses tumor growth in a xenograft model of renal cell carcinoma by inhibiting the activation of NF-κBonlinelibrary.wiley.com...

Immunohistochemistry and Western blot analysis showed decreased nuclear localization of NF-κB and phosphorylated NF-κB protein and subsequently
expression of MMP-9, Bcl-xL and Cox-2 in response to parthenolide treatment. These results indicate that parthenolide is a useful in the treatment of
renal cell carcinoma and acts via inhibition of NF-κB.

The roots, stems and leaves are antiphlogistic, antirheumatic, depurative and tonic[147, 218]. A decoction of the roots and stems is used
internally whilst the crushed fresh leaves are used for external applications[147]. The plant is used in the treatment of paralysis, numbness of the
four extremities, headache, toothache, spontaneous abscess formation and snake bites[147]. Many plants in this genus contain compounds of interest for
their antitumour activity[218]. Plants for a Future Database

Several active ingredients: one being Celastrol, which is also found in the related Chinese vine: Tripterygium Wilfordii. en.wikipedia.org...

A New Sesquiterpene Ester from Celastrus orbiculatus Reversing Multidrug Resistance in Cancer Cellspubs.acs.org...

In a search for revertants of multidrug-resistance in cancer cells, a novel (1) and two known (2, 3) sesquiterpene esters were isolated from the
root of Celastrus orbiculatus. The structure of 1 was elucidated as 1β,2β-diacetoxy-6α,9α-bis(benzoyloxy)dihydro-β-agarofuran. Compounds 1−3
partially or completely reversed resistance to adriamycin, vinblastine, and paclitaxel of multidrug-resistant KB-V1 and MCF7/ADR cells.

Antiinflammatory Constituents of Celastrus orbiculatus Inhibit the NF-κB Activation and NO Productionpubs.acs.org...

Two new sesquiterpene esters, 1β,8β-diacetoxyl-6α,9α-difuroyloxydihydro-β-agarofuran (1) and
1β-acetoxyl-2β,6α,9α-trifuroyloxydihydro-β-agarofuran (2), together with four known sesquiterpene esters (3−6), celastrol (7), and celaphanol A
(8) were isolated from the roots of Celastrus orbiculatus in a search for inhibitors of NF-κB activation and nitric oxide production. Compound 7 was
the most active, while compounds 1, 2, 4, and 8 showed moderate inhibition in both NF-κB activation and nitric oxide production.

Novel triterpene (12-oleanene-3beta, 6alpha-diol) from C. hypoleucus significantly inhibited proliferation of RKO cells in dose-dependent and
time-dependent manner, the IC50 was (12.20 +/- 0.79) microg x mL(-1) at 48 h. Typical apoptotic changes were observed in RKO cells under the
fluorescence microscope and the light microscope. DNA ladder was detected on agarose gels at concentrations from 10 microg x mL(-1) to 20 microg x
mL(-1) at 48 h. With FCM methods, dose-dependent apoptosis-induced effect was observed in RKO cell line after treatment of triterpene for 48 h, and
the apoptotic rates were increased from(2.93 +/- 0.84) % to (50.79 +/- 6.61) % at concentrations from 2.5 microg x mL(-1) to 20 microg x mL(-1). DNA
histograms data from FCM analysis showed that the number of cells was obviously reduced during G0-G1 phase and G2-M phase, but not during S phase for
RKO cell line after treatment with various concentrations of the triterpene for 48 hours.

Conclusion Both the extracts from Celastrus orbiculatus thunb with ethyl acetate and n-butanol induced the apoptosis of SGC-7901 cells in vitro by
a potential mechanism of up-regulating the expression of P53 gene.

Celastrol, a Triterpene Extracted from the Chinese “Thunder of God Vine,” Is a Potent Proteasome Inhibitor and Suppresses Human
Prostate Cancer Growth in Nude Micecancerres.aacrjournals.org...

Celastrol, an active compound extracted from the root bark of the Chinese medicine “Thunder of God Vine” (Tripterygium wilfordii Hook F.), was
used for years as a natural remedy for inflammatory conditions. Although Celastrol has been shown to induce leukemia cell apoptosis, the molecular
target involved has not been identified. Furthermore, whether Celastrol has antitumor activity in vivo has never been conclusively shown. Here, we
report, for the first time, that Celastrol potently and preferentially inhibits the chymotrypsin-like activity of a purified 20S proteasome (IC50 =
2.5 μmol/L) and human prostate cancer cellular 26S proteasome (at 1-5 μmol/L). ...Multiple assays using the animal tumor tissue samples from both
early and end time points showed in vivo inhibition of the proteasomal activity and induction of apoptosis after Celastrol treatment. Our results show
that Celastrol is a natural proteasome inhibitor that has a great potential for cancer prevention and treatment.

The results showed that GA could inhibit the proliferation and induce the apoptosis of the oral squamous cell carcinoma cell lines and that the
NF-kappa B pathway was simultaneously activated by GA treatment. The minimal cytotoxic dose of celastrol was able to effectively suppress the
GA-induced NF-kappa B pathway activation. Following the combined treatment with GA and the minimal cytotoxic dose of celastrol or the dominant
negative mutant SR-IκBα, proliferation was significantly inhibited, and the apoptotic rate of Tca8113 cells was significantly increased.
Conclusion
The combination of GA and celastrol has a synergistic antitumor effect. The effect can be primarily attributed to apoptosis induced by a decrease in
NF-kappa B pathway activation. The NF-kappa B signaling pathway plays an important role in this process. Therefore, combining GA and celastrol may be
a promising modality for treating oral squamous cell carcinoma.

The TMZ/CEL combination induced the phosphorylation of c-Jun NH2-terminal kinase, implicating the mitogen-activated protein kinase pathway in the
treatment effects. Our data suggest that CEL may be effective in sensitizing resistant melanoma cells to the effects of TMZ.

Citrus Auraptene Exerts Dose-dependent Chemopreventive Activity in Rat Large Bowel Tumorigenesis: The Inhibition Correlates with
Suppression of Cell Proliferation and Lipid Peroxidation and with Induction of Phase II Drug-metabolizing Enzymescancerres.aacrjournals.org...

These findings suggest that the inhibitory effects of auraptene on AOM-induced colon tumorigenesis at the initiation level might be associated, in
part, with increased activity of Phase II enzymes, and those at the postinitiation stage might be related to suppression of cell proliferation and
lipid peroxidation in the colonic mucosa.

The modifying effects of the organoselenium 1,4-phenylenebis(methylene)selenocyanate (p-XSC) and the Citrus antioxidant auraptene as dietary
supplements on experimental pulmonary metastasis of B16BL6 murine melanoma cells were investigated in an i.v. injection model in mice. ...These
results indicate that in mice, diet supplementation with p-XSC and auraptene reduces pulmonary metastasis of B16BL6 melanoma cells and inhibits the
growth of these metastatic tumors in lung, in part, by inducing apoptosis. We suggest that these agents, especially p-XSC, may be valuable in
preventing metastatic diseases in future studies in the clinic.

Suppression by citrus auraptene of phorbol ester- and endotoxin-induced inflammatory responses: role of attenuation of leukocyte activation
carcin.oxfordjournals.org...

Auraptene (AUR), a citrus coumarin derivative, is one of the promising chemopreventive agents against skin, tongue, esophagus and colon
carcinogenesis in rodents. We reported previously that AUR suppresses superoxide anion (O2–) generation from inflammatory leukocytes in in vitro
experiments. ...This contrasting activity profile between AUR and UMB was rationalized to be a result of their distinct differences in cellular uptake
efficiencies, i.e. the geranyloxyl group in AUR was found to play an essential role in incorporation. Thus, our findings indicate that AUR is an
effective agent to attenuate the biochemical responsiveness of inflammatory leukocytes, which may be essential for a greater understanding of the
action mechanism that underlies its inhibition of inflammation-associated carcinogenesis.

We here investigated the influence of nobiletin and auraptene on prostate carcinogenesis using transgenic rats developing adenocarcinoma of the
prostate (TRAP) bearing the SV40 T antigen transgene under control of the probasin promoter and human prostate cancer cells. ... A further experiment
demonstrated that growth of androgen sensitive LNCaP and androgen insensitive DU145 and PC3 human prostate cancer cells, was suppressed by both
nobiletin and to a lesser extent auraptene in a dose-dependent manner, with significant increase in apoptosis. In conclusion, these compounds,
particularly nobiletin, may be valuable for prostate cancer prevention.

In Vitro Absorption and Metabolism of a Citrus Chemopreventive Agent, Auraptene, and Its Modifying Effects on Xenobiotic Enzyme Activities
in Mouse Liverswww.ncbi.nlm.nih.gov...

Oral administration of AUR by gavage at 50-200 mg/kg body wt dose dependently induced glutathione S-transferase (GST) activity in mouse livers
without affecting cytochrome P-450 activity. Using 10 coumarin-related compounds, we found that only those coumarins having a 7-alkyloxyl group
induced GST, but not cytochrome P-450, activity. The present study presumes that AUR accumulates in the epithelial cells of the small intestine and
then gradually permeates into the portal vein. Stable localizability of AUR in the colon and liver may be associated with the induction of GST
activity, which is important as the action mechanism for suppression of rodent chemical carcinogenesis.

Dietary administration of auraptene significantly decreased BrdU-labelling index and polyamine concentrations in the oral mucosa (P < 0.05). In
addition, auraptene administration significantly increased the activities of GST and QR in the liver and tongue. Although dose-dependent effect was
not found, citrus auraptene is effective in inhibiting the development of oral neoplasms induced by 4-NQO. Thus, suppression by the initiation-feeding
of auraptene might relate to elevation in the phase II enzymes GST and QR of the liver and tongue, and inhibition occurring during the post-
initiation might be related to suppression of increased cell proliferation caused by 4-NQO in the oral mucosa.

Coumarin-related compounds, auraptene and umbelliferone, have been isolated from the cold-pressed oil of natsumikan (Citrus natsudaidai HAYATA),
and tested as inhibitors of tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced Epstein-Barr virus activation in Raji cells.
...Quantitative analyses using high-performance liquid chromatography showed the occurrence of auraptene not only in both the peels and sarcocarps of
natsumikan, but also in those of hassaku orange (C. hassaku) and grapefruit (C. paradisi,) and even in their bottled fresh juice form. These results
indicate that auraptene is a chemopreventer of skin tumorigenesis, and implies that suppression of leukocyte activation might be the mechanism through
which it inhibits tumor promotion.

The bottom line is that the best bet we have in treating cancer is with the current medical practice. To postpone that treatment by using alternative
therapies can be a death sentence. By all means, eat well, use preventative measures, but when the doctor says "This radiation treatment will cure
you", in my estimation, only a fool will decline and keep sucking back the ol' essiac, et al.

That is the point that fails to come forward in discussions like this, and probably kills more cancer patients than alternative proponents would care
to know about.

And if I have made that point, then that's all I need to say.

Your Joking right??

Lets say I own a Auto Shop, I have tons of people coming in for work which keeps me employed and I want to make sure it STAYS THAT WAY.

What would I do;
A. Fix problem and send them on their way never coming back for the same problem because I "Fixed" it.
B. "Fix" it only to make to make sure;
1: I "Fix" it and tell them later on that I tried by best when they return to spend more $$ due to failure.

2: Make it look like I fixed it but in reality issue a temporary fix insuring they will return for another fix, Certainly keeping a flow of income
for me.

Now replace Auto shop with Your Doctor or Cancer treatment facility/Cancer Treatment Centers of America and you have yourself a
never ending supply of Customers waiting to spend thousands and thousands of Dollars for your "Treatment"

Benchmark dose methods were used to estimate the ED10 and LED10 for olfactory degeneration, the precursor lesion thought to drive cellular
proliferation and eventually tumor development at excess cellular acetaldehyde levels. A concentration x time adjustment was applied to the benchmark
dose values. Human-equivalent concentrations were calculated by using the human PBPK model to predict concentrations that yield similar cellular
levels of acetic acid, acetaldehyde, and pHi. After the application of appropriate uncertainty factors, an ambient air value of 0.4 to 1.0 ppm was
derived. The biologically based approach supports a workplace standard of 10 ppm.

Differentiating between local cytotoxicity, mitogenesis, and genotoxicity in carcinogen risk assessments: the case of vinyl acetate
www.ncbi.nlm.nih.gov...

Vinyl acetate is carcinogenic at portals of entry (nasal cavity and upper gastrointestinal tract). Local metabolism of vinyl acetate produces
DNA-reactive acetaldehyde but also produces acetic acid and protons, which contribute to intracellular acidification, cytotoxicity and cell
proliferation.

Vinyl acetate is used in the manufacture of many polymers. The Clean Air Act Amendments of 1990 require that an inhalation risk assessment be
conducted to assess risks to human health from ambient exposures. Vinyl acetate is a nasal carcinogen in rats and induces olfactory degeneration in
rats and mice.

Chronic inhalation exposure to vinyl acetate (VA) causes lesions in the nasal cavity of the rat. This effect appears to be related to tissue
exposure to either acetaldehyde (AAld) or acetic acid (AA) metabolites of VA or both. ...The dosimetry model was applied to data from a series of
experiments designed to measure the uptake and metabolism of VA in the isolated upper respiratory tract of the rat at exposure concentrations ranging
from 73 to 2190 ppm. ...In addition, based on measured tissue hydrolysis rates, sufficient acid should be formed by the metabolism of VA to cause
significant changes in pHi. VA exposures of 200 and 600 ppm were predicted to result in a pHi of less than 7.2 and 6.7, respectively. This model
provides nasal dosimetry estimates needed to develop mechanistically based risk assessment approaches for human exposures to VA vapor.

Vinyl acetate was evaluated for chronic toxicity and oncogenicity in male and female rats and mice in a 104-week study. Target concentrations were
0, 50, 200, and 600 ppm. The study included interim terminations at approximately 53 and 83 weeks and a group whose exposure was terminated at 70
weeks and allowed a 15-week recovery period. Over the course of the exposures, body weight gain was consistently depressed in all 600 ppm groups and
in the 200 ppm mice. Except for female rats of the 600 ppm exposure group, recovery animals showed significant improvements in weight gain relative to
controls. There were no changes in hematological parameters of either species that could be unequivocally related to treatment. The only effect noted
on clinical chemical parameters during the study were decreases in blood glucose in the 600 ppm females. There were no adverse effects on survival in
either species. Increases in lung weight were noted in rats and mice primarily in the 600 ppm groups. These changes were associated with bronchial
exfoliation, macrophage accumulation, and fibrous plaques and buds extending into the airway lumen, and bronchial/bronchiolar epithelial
disorganization. The most significant histopathological changes were noted in the nasal cavity. In the olfactory epithelium of both rats and mice, the
main nonneoplastic changes included epithelial atrophy, regenerative effects (squamous metaplasia and respiratory metaplasia of olfactory epithelium),
basal cell hyperplasia, and epithelial nest-like infolds. No nonneoplastic changes were observed in the respiratory epithelium of rats, while squamous
metaplasia at the naso/maxilloturbinate region was prevalent in mice. Nonneoplastic changes were similar in the recovery groups. Oncogenic responses
to vinyl acetate exposure were mainly confined to the nasal cavity in rats and included endo- and exophytic papillomas, squamous cell carcinoma,
carcinoma in situ in olfactory regions, and endophytic papilloma in respiratory regions. Squamous cell carcinomas were also found either in areas
normally covered by cuboidal epithelium or areas of unknown origin. One squamous cell carcinoma was found in the larynx of a rat of the 600 ppm
groups. One squamous cell carcinoma was found in the lung of a mouse of the 600 ppm group. The no-observable- adverse-effect level for all effects was
50 ppm in both species. The tumorigenic response appears to be nonlinear. The nonlinear dose response and the unique nature of the rodent nasal cavity
suggest that specific risk extrapolation models should be developed for vinyl acetate.

In rats exposed to the high concentration of VA (600 ppm), Owen (1988) noted lesions at different levels in the respiratory tract. In the
histopathology report of Dreef-van der Meulen (1988) on Owen's animals, olfactory epithelial metaplasia/atrophy and nest-like epithelial folds
(hyperplastic, regenerative epithelial structures) were noted in the nasal cavity, exfoliation of bronchial epithelium, fibrous intraluminal
projections (also termed tags, indicative of regeneration of exfoliated areas) in the bronchi, and pigmented histiocyte accumulation in the lungs. No
alterations were noted in the trachea. Data presented in the study showed that these respiratory tract lesions all occurred in the high-exposure
animals with increased severity or at incidences significantly greater than in controls (p

While it isn't that mechanics need to operate like that, all too many of them do.

Everyone who owns a car has experienced that, even if they don't know it.

Why would this be any different with the medical establishment?

I don't know about anyone else, but I regularly tell my customers where to find the info that they can figure out how to fix a better part of the
niche machines after we sell it to them or do a major overhaul for them. Nobody wants to buy money pits... but then again mechanics and doctors know
we need automobiles and health, regardless. While it doesn't cost $10,000 a day for me to work on someones machine, from my point of view it's still
expensive. I feel grimy if they're paying for the most menial marginal things, while eventually sorts of things will break that they have to bring it
in to the pros.

I don't joke much about cancer and if one has never faced the beast, one never knows the road they'll take. Your analogies are all very well and
good until things get serious. If you should happen to get to that point...

If you have lung or related respiratory types of cancer then house plants should be a must. Plants filter toxic agents such as benzene, formaldehyde
and trichloroethylene from the air, and emit oxygen which may help with Tumor Hypoxia.

1. There are physicians willing to work with patients in using natural products alone or in conjunction with conventional surgery, chemotherapy, etc.
You can find them via various websites. One I like is the American Academy of Antiaging Medicine's fellowship on Integrative Cancer Treatment.
They can refer you to a graduate of their program.

2. The problem with poor adoption of these natural chemicals is that they are not patentable. Politically, I think it would greatly improve cancer
care if we were to grant companies the ability to patent such products for a limited time period, say 20 years, providing that they actually sold it
on the market-not just held the patent and prevented others from making it. Companies are not intrinsically evil; they just want to make money. If
you make it profitable, the big pharma companies will jump right onto the natural product manufacturing business and doctors will use them. Patent
law is the problem; there is no conspiracy. Doctors are mostly trained to use what is promoted by drug companies.

3. What works in a lab does not always work in a human being. Many things kill cancer cells in a petrie dish, but due to lack of absorption or other
factors when they are eaten, they may do nothing in a living human. So, when evaluating compounds, one must look for substances that have shown
results in actual living cancer patients, such as melatonin, fish oil, curcumin, etc. Perhaps if they could be given intravenously a better effect
would be seen. However, most of these products are only available as oral preparations.

4. I am a physician and use many of these products in my practice of integrative medicine. The are are best for prevention and
post-surgery/post-chemo recurrence prevention. They are not magic bullets. The best option, in my experience, is to combine them with a rigid
diet/juicing regimen such as Gerson therapy, a detox program including removal of heavy metals etc which is quite complex and beyond the scope of this
site, and low dose targeted chemotherapy using a variety of natural or synthetic drugs chosen via sophisticated chemo-sensitivity testing, not
available in the US, and then IPT (insulin-potentiation therapy), and enhancement of immune functioning with things like D-fraction, Beta-glucan, etc.
I have seen complete cures of "terminal" cancer patients, including the physician to whom I refer patients for all of this(cured his own lung
cancer). It works, but is currently very expensive and mostly not paid by insurance, and requires the patient to drastically change their diet and
lifestyle forever-or the cancer may recur. Most people get cancer because of their terrible diet and lifestyle choices; they may be willing to change
for a short time, but not long term in most cases. If they can't maintain the new diet/supplements, the cancer recurs as it is a systemic condition,
not just an isolated thing that can be plucked out.

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